Endocrine Function of the Pancreas and Gastrin Secretion in Patients with a Kidney Transplant&lt;sup&gt;1&lt;/sup&gt;

Żukowska-Szczechowska, E; Grzeszczak, W; Kokot, F; Nieszporek, Teresa; Kuśmierski, S; Szkodny, A

doi:10.1159/000185835

Cited by 2 publications

(5 citation statements)

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“…We found no significant differences in the test meal induced response of glucagon be tween KTP treated with azathioprine or CS-A. respectively [56]. The importance of ele vated basal plasma glucagon levels in the pathogenesis of carbohydrate intolerance in KTP remains to be elucidated.…”

Section: Glucagonmentioning

confidence: 53%

“…After suc cessful renal transplantation baseline levels are in the normal range, showing a significially reduced response to a test meal [56]. No significant differences in the test meal induced pancreatic polypeptide profile be tween CS-A-and azathioprine-treated KTP were found [56].…”

Section: Pancreatic Polypeptidementioning

confidence: 98%

“…Hyperinsuiinism is considered to be involved in the pathogen esis of hypertriglyceridaemia in uraemic pa tients. In KTP, carbohydrate intolerance may persist in spite of normal [56,57] or even elevated [58] plasma insulin levels. In addition, the response of plasma insulin to a test meal is significantly reduced as com pared with normals [56] and more markedly in CS-A-than azathioprine-treated patients [56].…”

Section: Insulinmentioning

confidence: 99%

“…In KTP, carbohydrate intolerance may persist in spite of normal [56,57] or even elevated [58] plasma insulin levels. In addition, the response of plasma insulin to a test meal is significantly reduced as com pared with normals [56] and more markedly in CS-A-than azathioprine-treated patients [56]. It seems that carbohydrate intolerance or even overt diabetes mellitus in KTP are due predominantly to the diabetogenic ac tion of glucocorticoids [56], The importance of CS-A in the pathogenesis of suppressed insulin secretion is very likely, as a suppres sive effect of CS-A on the insulin release by the pancreatic islet was demonstrated [59],…”

Section: Insulinmentioning

confidence: 99%

“…The patho physiologic importance of increased glucagonaemia in CRF is quetionable. After suc cessful renal transplantation baseline plasma glucagon levels are elevated [56] and normal [60] and normally responsive to a test meal. We found no significant differences in the test meal induced response of glucagon be tween KTP treated with azathioprine or CS-A.…”

Section: Glucagonmentioning

confidence: 99%

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Endocrine Alterations in Kidney Transplant Patients

Kokot¹,

Grzeszczak²,

Żukowska-Szczechowska³

et al. 1990

Blood Purif

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Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: (1) duration of chronic uraemia before renal transplantation; (2) residual function of the patients’ native kidneys; (3) quality of function of the renal graft; (4) modulation of secretion, transport, and degradation of hormones, and/or (5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.

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Section: Glucagonmentioning

confidence: 53%

Section: Pancreatic Polypeptidementioning

confidence: 98%

Section: Insulinmentioning

confidence: 99%

Section: Insulinmentioning

confidence: 99%

Section: Glucagonmentioning

confidence: 99%

See 3 more Smart Citations

Endocrine Alterations in Kidney Transplant Patients

Kokot¹,

Grzeszczak²,

Żukowska-Szczechowska³

et al. 1990

Blood Purif

Self Cite

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Islet cell responses to glucose in human transplanted pancreas

Elahi

Clark

McAloon-Dyke

et al. 1991

American Journal of Physiology-Endocrinology and Metabolism

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Postsurgery, pancreas transplantation results in alterations of carbohydrate metabolism. Additionally, immunosuppressive therapy impacts on glucose regulation. We evaluated the hormonal and metabolic responses of pancreas allografts, utilizing the hyperglycemic clamp technique coupled with the tritiated glucose methodology, in 11 volunteers who had received simultaneous pancreas-kidney transplantation (P-K) with systemic drainage. Their responses were compared with seven volunteers who had received only a kidney (K) graft and with seven normal control (C) volunteers. Although basal glucose and hepatic glucose output were similar in all three groups, basal insulin, C-peptide, glucagon, and pancreatic polypeptide were highest in the P-K group and lowest in normal subjects. During hyperglycemia, all groups showed a similar characteristic, initial complete suppression of hepatic glucose production, with recovery followed by a later suppression. Peripheral glucose uptake was similar in P-K and C subjects but decreased in K patients. Systemic insulin levels were fourfold higher in the pancreas transplant patients than in healthy subjects. Thus, under basal and hyperglycemic stimulation, 1) hepatic glucose homeostasis is regulated normally, even with pancreatic drainage into the systemic circulation; 2) overall glucose disposal is normal in P-K patients because of marked hyperinsulinemia; and 3) there is loss of tonic inhibition of endocrine pancreatic function secondary to pancreatic denervation.

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Endocrine Function of the Pancreas and Gastrin Secretion in Patients with a Kidney Transplant<sup>1</sup>

Cited by 2 publications

References 2 publications

Endocrine Alterations in Kidney Transplant Patients

Endocrine Alterations in Kidney Transplant Patients

Islet cell responses to glucose in human transplanted pancreas

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